Journal
JOURNAL OF MOLECULAR BIOLOGY
Volume 428, Issue 17, Pages 3399-3407Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2016.05.023
Keywords
Type 3 secretion system, EspG; host-pathogen interactions; small GTPase signaling; endosomal recycling; cargo trafficking
Categories
Funding
- Medical Research Council
- Royal Society
- MRC [MR/J006874/1, MR/K019007/1] Funding Source: UKRI
- Medical Research Council [MR/J006874/1, MR/J006874/1B, MR/K019007/1] Funding Source: researchfish
- Wellcome Trust [107057/Z/15/Z] Funding Source: researchfish
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Enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC/EHEC) manipulate a plethora of host cell processes to establish infection of the gut mucosa. This manipulation is achieved via the injection of bacterial effector proteins into host cells using a Type III secretion system. We have previously reported that the conserved EHEC and EPEC effector EspG disrupts recycling endosome function, reducing cell surface levels of host receptors through accumulation of recycling cargo within the host cell. Here we report that EspG interacts specifically with the small GTPases ARF6 and Rab35 during infection. These interactions target EspG to endosomes and prevent Rab35-mediated recycling of cargo to the host cell surface. Furthermore, we show that EspG has no effect on Rab35-mediated uncoating of newly formed endosomes, and instead leads to the formation of enlarged EspG/TfR/Rab11 positive, EEA1/Clathrin negative stalled recycling structures. Thus, this paper provides a molecular framework to explain how EspG disrupts recycling whilst also reporting the first known simultaneous targeting of ARF6 and Rab35 by a bacterial pathogen. (C) 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
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